INTRODUCTION:

Using oils from exotic and native vegetables is a trend in the current cosmetic field. Previously, Rennert and Melzig¹ demonstrated that saturated and unsaturated free fatty acids (C₁₂ - C₂₂) presented inhibitory activity on collagenase and elastase, highlighting in this group the following fatty acids: palmitic, stearic, myristic, heptadecanoic, palmitoleic, oleic, linoleic, and linolenic.

The cañihua seeds present an oil with a high percentage of unsaturated and saturated fatty acids, which confers an essential use in cosmetics.

These fatty acids could inhibit the collagenase and elastase enzymes, reduce the oxidation of the cellular structures, increase the resistance against oxidative stress, and prevent the synthesis of metalloproteinases, which allows for reducing skin aging².

During aging, the dermis undergoes the most evident changes due to the breakdown and irregular distribution of collagen, the main component of the extracellular matrix (ECM), and decreases due to the action of metalloproteinases (MMPs) and impaired signalling of transforming growth factor β (TGF-β) due to the action of reactive oxygen species (ROS), which hinders the mechanical interaction between fibroblasts and the ECM, impairing fibroblast function. Other components of the ECM affected by the aging process are elastic fibers, glycosaminoglycans (GAGs), and proteoglycans (PGs), which implies the reduction of the functional components of the dermis, resulting in the appearance of clinical signs of aging³.

Chronic solar radiation is usually cumulative and can trigger macroscopic and microscopic changes that can be evidenced at the cellular and molecular levels of the skin. Photodamage is produced primarily by the production of reactive oxygen species (ROS) that cause oxidation of cellular components; in addition, UV rays indirectly stimulate the transcription of genes that encode the synthesis of metalloproteinase enzymes (collagenase and elastase), enzymes that degrade the proteins of the dermal extracellular matrix, primarily collagen, and elastin⁴.

Plant derivatives have been a popular ingredient in cosmetics for centuries due to their natural and harmless properties. Nowadays, herbal cosmetics, which can be used as cosmeceuticals⁵, have become increasingly popular as they are believed to have no side effects, unlike synthetic cosmetics. They can reduce skin damage caused by oxidative stress, slow aging, and enhance skin functions. Herbal cosmetics use various plant-derived ingredients with antioxidant, anti-aging, anti-inflammatory, and antiseptic properties⁶.

Cosmeceuticals are hybrid products that improve the skin's health and appearance. They contain functional ingredients that treat various skin conditions, boost collagen growth, neutralize free radicals, and maintain the keratin structure⁷.

In this regard, the cosmetic industry, considering the current worldwide trend of using natural cosmetic actives, has been looking for potential products that contribute to controlling photodamage and delaying skin aging caused by a decrease in collagen synthesis or an increase in its degradation due to collagenase activation. Therefore, many studies on skin aging prevention focus on inhibiting collagenase and elastase synthesis and increasing collagen or elastin production⁸. Some topically applied oils are known to improve skin elasticity and maintain water retention capacity and hydration by restoring barrier function and exerting an antioxidant effect.

Considering that cañihua oil has unsaturated and saturated fatty acids in its composition, it is intended to corroborate its potential use as a skin protector.

The main objective of this research was to evaluate the antioxidant, anticollagenase, and antielastase activity of Chenopodium pallidicaulle "cañihua" oil. As a strategy, in vitro evaluation methods were used, which allowed us to determine its potential use in the formulation of anti-photoaging cosmetics. We also tried to achieve an added value for the oil of this Peruvian Andean grain.

MATERIALS AND METHODS:

Materials:

2,2-Diphenyl-1-picrylhydrazyl (DPPH), ascorbic acid, 2,2′-azino-bis-3-ethylbenzthiazoline-6-sulphonic acid (ABTS), potassium persulfate (K₂S₂O₈), trolox, epigallocatechin gallate (EGCG), N-[3-furylacryloyl]-Leu-Gly-Pro-Ala (FALGPA), N-succinyl-Ala-Ala-p-nitroanilide (SANA), Tris(hydroxymethyl) aminomethane (Tris base buffer), tricine buffer, enzyme elastase (EC 3.4.21.36) from porcine pancreas, collagenase (EC 3.4.24.3) from Clostridium histolyticum type IA were obtained from Sigma-Aldrich. Hexane and dimethyl sulfoxide (DMSO) were obtained from Merck.

Samples preparation:

Chenopodium pallidicaule seeds were obtained from the rural community of Sillarani, department of Puno, Perú. The specimen was identified at the Vargas Cuz Herbarium at Universidad Nacional de San Antonio Abad del Cusco. The seeds were previously grounded to a particle size of 1 mm in a Foss cyclone mill, model CT293 Cyclotec.

Extraction of Chenopodium pallidicaule seeds oil:

A supercritical fluid extraction equipment, model MV-10 ASFE® from Waters Corporations, was used for extraction under the following conditions: pressure (200 bar), extraction time (60 min), temperature (45°C), and CO₂ Flux (4 mL/min).

Identification and quantification of the primary fatty acids:

The fatty acid profile of cañihua oil was established according to AOAC Official Method 948.22⁹. 100 mg of oil was dissolved in 10 mL of hexane, then 2 mL of 2N sodium hydroxide (methanolic solution) was added, shaken vigorously, and centrifuged. Analysis was performed on the supernatant with a 6890 N Network GC gas chromatography system (Agilent Technologies, Santa Clara, CA, USA) coupled to a mass spectrometry detector. FAMEs were separated using a 50 m x 0.35 mm x 1.05 μm thick column. The carrier gas was helium with a 0.6 mL/min flow rate. The injector and detector were conditioned at 250°C and 270°C, respectively. The injection volume of 0.5 μL was performed in Split mode (100:1). FAMEs were separated by GC, fragmented by Mass spectrometer, and identified by comparing mass spectra with the NIST library¹⁰. Fatty acid (FA) content was expressed as % w/w (g FA/100 g sample).

2,2-diphenyl-1-picrylhydrazyl (DPPH) radical inhibition assay.

The antioxidant activity of Chenopodium pallidicaule oil was determined using the method proposed by Gali and Bedjou¹¹. Dilutions of the oil (12.5 - 150 mg/mL) were prepared using dimethyl sulfoxide (DMSO). 40 μL of each oil dilution was mixed with 160 μL of a methanolic solution of 0.1mM DPPH in a 96-well microplate and incubated for 30 minutes at room temperature in the dark. Ascorbic acid (1 mg/mL) was used as a positive control. After 30 minutes, absorbance readings were taken at 517 nm using a microplate reader (Absorbance microplate reader EPOCH 2, Biotek, Germany). Experiments were performed in duplicate. The percentage inhibition of DPPH was estimated with the following equation:

Abs. control – Abs. sample

% inhibition of DPPH = ------------------------------ X 100

Abs. control

(1)

Where:

Abs. control is the absorbance of the mixture containing DPPH and DMSO solvent.

Abs. sample is the absorbance of the mixture containing DPPH and the oil dilutions.

The IC₅₀was obtained from the line obtained by plotting the percentage of antioxidant activity versus the sample concentration (mg/mL).

2,2-azino-bis-3-ethylbenzthiazoline-6-sulfonic acid (ABTS) assay:

The percentage inhibition of the ABTS radical was determined using the method followed by Yeerong et al.¹².

The ABTS^●+ radical was obtained after reacting a 7 mM ABTS solution with a 2.45 mM potassium persulfate (K₂S₂O₈) solution in a 2:3 ratio. This mixture was left at room temperature (± 25°C) for 16 hours in the dark. This ABTS^●+ radical was diluted with ethanol to an absorbance of 0.70 (± 0.1) at 734 nm. Dilutions of the oil (12.5 - 100 mg/mL) were prepared using dimethyl sulfoxide (DMSO). 20 μL of each oil dilution was mixed with 180 μL of ABTS^●+ solution in a 96-well microplate and incubated for 30 min at room temperature and in the dark. Trolox (1 mg/mL) was used as a positive control. Absorbance readings were made at 734 nm using a microplate reader (Absorbance microplate reader EPOCH 2, Biotek, Germany). The percentage inhibition of ABTS^●+ was calculated using equation (1) described in the DPPH method; the mean inhibition concentration (IC₅₀) was also established in the respective graph of the percentage of antioxidant activity versus sample concentration (mg/mL).

Anticollagenase activity:

The assay used to determine the inhibitory activity of collagenase was based on the spectrophotometric method described by Thring et al.¹³ with some modifications in a microplate reader (Absorbance microplate reader EPOCH 2, Biotek, Germany). The kit for colorimetric assay of collagenase activity of Clostridium histolyticum (MAK293-1KT) was used, having a concentration of 0.35 units/mL according to the activity data of the supplier. The oil (1.5 - 50 mg/mL) was diluted using DMSO. For the assay, 20 μL of each dilution and 20 μL of collagenase solution were added and incubated at 37°C for 15 minutes. Then, 80 μL of collagenase assay buffer and 40 μL of FALGPA substrate were added. The absorbance reading at 340 nm was performed. Epigallocatechin gallate (EGCG) was used as a positive control. The percentage of enzymatic inhibition was calculated with the following equation:

Abs. control – abs . sample

% enzyme inhibition = --------------------------------X 100

Abs. control

(2)

Where:

Abs. control is the mixture of DMSO, collagenase solution, tricine buffer, and FALGPA substrate.

Abs. sample is the mixture of the dilutions of the oils, collagenase solution, tricine buffer, and FALGPA substrate.

The mean inhibitory concentration (IC₅₀) was calculated using the dose-response curve equation. The assays were performed in duplicate.

Anti-elastase activity:

The assay was based on using porcine pancreatic elastase (E-1250). The substrate N-succinyl-Ala-Ala-AlaAla-p-nitroanilide (AAAPVN) was dissolved in a buffer at 0.8 mM. Dilutions of the oil (12.5 - 300 mg/mL) were performed using DMSO. For the assay, 10 μL of each dilution was used, 40 μL of elastase solution (0.1 U/mL) was added and incubated at 37°C for 15 min. Then 50 μL of Tris-HCl buffer (200 mM; pH=8) and 100 μL of AAAPVN substrate (0.8 mM) were added. Absorbance readings were taken at 410 nm. Epigallocatechin gallate (EGCG) was used as a positive control. The percentage of enzyme inhibition was calculated using equation (2)¹³.

Where: control is the mixture of DMSO, elastase solution, Tris-HCl buffer, and AAAPVN substrate, and the sample is the mixture of the dilutions of oils, elastase solution, Tris-HCl buffer, and AAAPVN substrate.

The mean inhibitory concentration (IC₅₀) was calculated using the dose-response curve equation. Assays were performed in duplicate.

Statistical analysis:

Statistical analysis was performed by using one-way analysis of the variance (ANOVA) followed by Tukey’s post hoc test to compare means showing significant differences (p<0.05).

RESULT AND DISCUSSION:

Extraction of oil from Chenopodium pallidicaule seeds:

Supercritical fluid extraction yielded 13.04% oil from Chenopodium pallidicaule seeds.

Identification and quantification of the primary fatty acids:

The chromatographic profile of the cañihua oil extracted by supercritical fluids was obtained through gas chromatographic coupled to mass spectrometry analysis, with a total of 15 peaks corresponding to the respective methyl ester derivatives of the fatty acids identified, as shown in Table 1.

Table 1. Quantification of fatty acids present in cañihua oil extracted with supercritical CO₂.

Peak	Chemical nomenclatura	Fatty acid	Average ± D. S
1	C18:2	Linoleic acid	46.66 ± 0.03
2	C18:3	Linolenic acid	5.31 ± 0.02
		Polyunsaturated fatty acids	51.97 ± 0.05
3	C18:1	Oleic acid	25.69 ± 0.00
4	C18:1	Elaidic acid	1.23 ± 0.03
5	C20:1	Gondoic acid	0.97 ± 0.01
6	C22:1	Erucic acid	0.67 ± 0.01
7	C16:1	Palmitoleic acid	0.08 ± 0.01
		Monounsaturated fatty acids	28.64 ± 0.06
8	C16:0	Palmitic acid	15.20 ± 0.01
9	C18:0	Stearic acid	1.26 ± 0.01
10	C20:0	Arachidic acid	0.61 ± 0.03
11	C22:0	Behenic acid	0.36 ± 0.01
12	C17:0	Isostearic acid	0.26 ± 0.01
13	C21:0	20-methyl-heneicosanoic acid	0.24 ± 0.02
14	C14:0	Myristic acid	0.12 ± 0.00
		Saturated fatty acids	18.05 ± 0.09
15		Squalene	1.34 ± 0.02
		Saturated fatty acids	18.05 ± 0.09
		Unsaturated fatty acids	80.61 ± 0.10

Table 1 shows that the primary fatty acid in C. pallidicaule seed oil was linoleic acid (46.66 ± 0.03%), followed by oleic acid (25.69 ± 0.00%), palmitic acid (15.20 ± 0.01%) and linolenic acid (5.31 ± 0.02%). Other fatty acids in smaller proportion were stearic acid (1.26 ± 0.01%), elaidic acid (1.23 ± 0.03%), gondoic acid (0.97 ± 0.01%), erucic acid (0.67 ± 0.01%), arachidic acid (0.61 ± 0.03%), behenic acid (0.36 ± 0.01%). This oil has a high percentage of unsaturated fatty acids (80.61 ± 0.10%) compared to saturated fatty acids (18.05 ± 0.09%).

Many vegetable oils from seeds contain essential fatty acids. For example, the oil from Cucurbita moschata seeds has linoleic acid as the primary fatty acid (51.74%), followed by oleic acid (28.64%), palmitic acid (12.36%), stearic acid (6.05%), and traces of behenic, arachidic, heptadecanoic, and eicosenoic acids¹⁴.

Orsavova et al.¹⁵ reported that the main fatty acids in sesame seed oil were oleic acid (41.5%), linoleic acid (40.9%), palmitic acid (9.7%), and stearic acid (6.5%). Eicosenoic, α-linolenic, behenic, and palmitoleic fatty acids were found in amounts less than 1%.

Black radish seed oil was analyzed to contain oleic acid (31.98 ± 0.53%) and linoleic acid (21.65 ± 0.46%), and low amounts (less than 1%) of eicotrienoic, eicosadienoic, eicosanoic, lignoceric, and palmitoleic fatty acids were reported¹⁶.

The analysis of sunflower oil showed that linoleic acid (49.52 ± 0.73%) is an essential part of its fatty acid composition, followed by oleic acid (38.81 ± 0.65%). Other detectable fatty acids were eicosenoic, eicotrienoic, erucic, and behenic acids, whose amounts are less than 1%¹⁶.

Fibrous hemp seed oil showed linoleic acid (56.05 ± 0.84%) and α-linolenic acid (20.49 ± 0.72%) as the main fatty acids, and eicosadienoic, eicosanoic, eicosenoic, and behenic acids were also detected in amounts less than 1%¹⁷.

Some different safflower cultivars' oil content and fatty acid composition ranged from 27.3% to 39.4%. Oleic acid was the primary monounsaturated fatty acid (11.2%—25.3%), while linoleic acid was the only polyunsaturated fatty acid (49.5%—82.4%). Palmitic acid content varied between 1.3% and 8.1%. Trace amounts of myristic acid were also detected¹⁸.

The fatty acids most found in all vegetable oils are oleic, linoleic, stearic, and palmitic. Oleic and linoleic fatty acids are present in most vegetable oils. The composition of C. pallidicaule seed oil and the reported seed oils is similar. On the other hand, the presence of squalene in C. pallidicaule seed oil was determined to be 1.34 ± 0.02%. Squalene is a polyunsaturated triterpene that is similar in structure to various vitamins. It is naturally found in amaranth seeds, rice bran, wheat germ oil, and shark liver oil¹⁹, and it has an essential role as a biosynthetic precursor of steroids in plants and animals. It is widely used as an essential ingredient in skin cosmetics²⁰. The squalene content in some commercially important oils, such as cottonseed, rice bran, peanut, sunflower, corn, olive, rapeseed, and cottonseed, was determined between 0.01 and 0.4%²¹. In the case of Amaranthus seed oil, the squalene content was reported to be 2.4 – 8.0%^22,23. The squalene detected in the present study was lower than Amaranthus oil but higher than other vegetable oils.

Figure 1 presents the mass spectrum of the main fatty acids identified and quantified, showing the formula and the mass for each.

Figure 1. Mass spectrum of palmitic acid methyl ester; 270 m/z (a), oleic acid methyl ester; 296 m/z (b), linoleic acid methyl ester; 294 m/z (c) and linolenic acid methyl ester; 292 m/z (d).

Antioxidant activity evaluation:

The antioxidant activity of C. pallidicaule oil was determined by DPPH and ABTS assays²⁴. The oil at the concentrations of 12.5, 25, 50, 100, and 150 mg/mL significantly increased the DPPH inhibition percentage by 4.47 ± 0.17, 11.91 ± 2.56, 25.98 ± 0.25, 45.87 ± 3.13, and 64.95 ± 2.02%, respectively (Figure 2A). Similarly, at the same concentrations except 150 mg/mL, the oil showed ABTS inhibition percentages of 10.93 ± 0.90, 23.06 ± 0.44, 34.58 ± 1.29, and 60.49 ± 0.42%, respectively (Figure 2B).

Figure 2. The effect of Chenopodium pallidicaule oil on the percentage of DPPH (A) and ABTS (B) scavenging.

(* p<0.05 indicates significant differences, as Tukey’s test indicates).

As shown in Table 2, C. pallidicaule oil inhibited DPPH (A) and ABTS (B) with IC₅₀ values of 112.06 ± 0.47 and 78.9 ± 0.14 mg/mL, respectively. This inhibition activity has been compared with ascorbic acid (0.0243 ± 0.21 mg/mL) and Trolox (0.00351 ± 0.32 mg/mL), respectively. It is important to note that the antioxidant activity of C. pallidicaule oil is lower than that of the standard antioxidants. Understanding that these are pure substances with a different antioxidant mechanism than fixed oils is crucial.

Table 2. Antioxidant activity of C. pallidicaule oil expressed as IC₅₀.

Method	IC₅₀(mg/mL) *
DPPH	Chenopodium pallidicaule oil	112.06 ± 0.47^a
DPPH	Ascorbic acid	0.0243 ± 0.21^c
ABTS	Chenopodium pallidicaule oil	78.9 ± 0.14^b
ABTS	Trolox	0.00351 ± 0.32^d

*Different letters indicate significant differences as indicated by Tukey’s test, at p<0.05

Oxygen species and free radicals can start the peroxidation of important unsaturated lipids in bio-membranes. This process is linked to many chronic health problems, such as aging, cancer, and atherosclerosis. It can also cause damage to the liver, kidney, and other organs and lead to inflammatory disorders, gastric ulcers, and destruction of proteins and nucleic acids, which can ultimately cause a decrease in cellular activity and living function^25,26.

Antioxidants prevent substrates from oxidizing by stabilizing or deactivating free radicals. They play a critical role in maintaining optimal cellular and systemic health²⁷.

Antioxidants protect humans against degenerative diseases and infections by inhibiting and scavenging free radicals²⁸.

In the study developed by Hong et al.²⁹, an IC₅₀ of 10.7 mg/ mL was obtained in the DPPH assay for Cannabis sativa oil. In another study, Dabbour et al.³⁰ reported an IC₅₀ of 3.34 mg/mL for milk thistle seed oil. Laghouiter et al.³¹ showed an IC₅₀ in the 46.42 ± 0.14 - 77.58 ± 0.27 mg/mL for oil from nine palm (Phoenix dactylifera L) seed cultivars. Mohammed et al.³² found an IC₅₀ of 205.15 - 248.16 mg/mL in the DPPH assay for virgin coconut oil.

In the present study, an IC₅₀ value of 112.06 ± 0.47 mg/mL was determined, a value that, compared to previous studies, is higher than that reported for Cannabis sativa, Milk thistle, and Phoenix dactylifera (palm) oils and lower than that reported for virgin coconut oil.

Wang et al.³³ found an IC₅₀ of 2.48 mg/mL for olive oil and 4.01 mg/mL for peanut oil using the ABTS inhibition method. Karrar et al.³⁴, found an IC₅₀ of 23.30 mg/mL for Cucumis melo var. Tibish. seed oil. According to Karrar et al.³⁵ the seed oil of gurum (Citrullus lanatus var. Colocynthoide), a melon species, extracted by supercritical fluids presented the highest ABTS inhibition capacity with an IC₅₀ of 28.14 mg/mL, followed by screw press extraction with an IC₅₀ of 31.91 mg/mL and hexane extraction with an IC₅₀ of 37.29 mg/mL, indicating that the type of extraction has a significant influence on the percentage of ABTS inhibition.

Bandara et al.³⁶ reported an IC₅₀ of 340.28 ± 1.23 mg/mL for ABTS for tropical almond oil (Terminalia catappa L.), and in the work developed by Muangrat and Jirarattanarangsri³⁷, a wide range of IC₅₀ was obtained for Camellia sinensis var. In Assamica oil in the ABTS assay, an interval of 9.65 ± 0.19 - 979.90 ± 44.21 mg/mL was reported, and it seems that some extraction conditions (T°, time, and pressure) influence the ABTS inhibition capacity.

In the present investigation, an IC₅₀ value of 78.9 ± 0.14 mg/mL was obtained, which, compared with other studies, is higher than that reported for white rice bran oil, mahua seed oil, olive oil, Cucumis melo var. Tibish and gurum were lower than those reported for tropical almond oil (Terminalia catappa) and Camellia sinensis var. Assamica oil was extracted at 40°C, 5 hours, and 175 bar (979.90 ± 44.21 mg/mL).

Anticollagenase and antielastase activity:

The inhibitory activities of collagenase and elastase were developed at different concentrations for collagenase inhibition used at concentrations of 1.5, 3, 6, 12.5, 25, and 50 mg/mL. It significantly increased the inhibition percentage of 7.67 ± 0.152, 17.11 ± 5.380, 28.09 ± 4.167, 36.06 ± 0.818, 41.54 ± 1.822, and 51.84 ± 1.249%, respectively (Figure 3C). On the other hand, for the elastase inhibition assay were used concentrations of 12.5, 25, 50, 100, 200, and 300 mg/mL significantly increased the inhibition percentage of 7.90 ± 5.595, 12.60 ± 5.084, 16.72 ± 5.862, 27.13 ± 4.532, 44.38 ± 1.903 and 57.55 ± 3.269%, respectively (Figure 3D).

(C)

(D)

Figure 3. Inhibition of collagenase (C) and elastase (D) activities.

(* p<0.05 indicates significant differences, as Tukey’s test indicates).

As shown in Table 3, C. pallidicaule oil inhibited the collagenase and elastase activities with IC₅₀ values of 42.87 ± 4.76 mg/mL and 244.22 ± 17.30 mg/mL, respectively. The inhibitory activity of C. pallidicaule oil on collagenase and elastase enzymes has been compared to that of Epigallocatechin gallate (0.059 ± 0.21 mg/mL and 0.014 ± 0.02 mg/mL), a potent inhibitor of both enzymes. It was found that C. pallidicaule oil has lower inhibitory activity on these enzymes compared to Epigallocatechin gallate, a pure substance with higher inhibitory activity on both enzymes.

Table 3. Inhibition of collagenase and elastase of C. pallidicaule oil expressed as IC₅₀

Biological activity	IC₅₀(mg/mL) *
Collagenase inhibition	Chenopodium pallidicaule oil	42.87 ± 4.76 ^a
Collagenase inhibition	Epigallocatechin gallate	0.059 ± 0.21^c
Elastase inhibition	Chenopodium pallidicaule oil	244.22 ± 17.30^b
Elastase inhibition	Epigallocatechin gallate	0.014 ± 0.02^d

*Different letters mean significant differences, as Tukey’s test indicates (p<0.05).

Dhawan and Nanda³⁸ reported an IC₅₀ of 4 mg/mL and 309 mg/mL for collagenase and elastase inhibition, respectively, for pomegranate seed oil. In the study by Kayath et al.³⁹, an IC₅₀ of 7.34 mg/mL and 42.3 mg/mL for collagenase and elastase inhibition was obtained for rosehip seed oil.

The work developed by Rennert and Melzig¹ showed the results of the systematic investigation of 17 free fatty acids (saturated and unsaturated, C₁₂-C₂₂) and their inhibitory effects on collagenase from Clostridium histolyticum and elastase from human neutrophils. Most fatty acids (except lauric, behenic, eicosapentaenoic, and docosahexaenoic) inhibit collagenase and elastase. The most potent inhibitory fatty acids for collagenase were the saturated fatty acids C₁₆ - C₁₉. In the case of elastase, the unsaturated fatty acids, such as oleic or linoleic, had higher inhibitory activity than saturated ones. Erucic acid was the most effective fatty acid on elastase inhibition.

Vegetable oils rich in essential fatty acids can increase collagen production and reduce the number of inflammatory cells in the wound-healing process⁴⁰. Some of them, such as palmitic, oleic, and stearic acids, are synthesized in the body. Still, linoleic acid is not synthesized, and its deficiency causes dry and flaky skin, cracked nails, increased hair loss, and transepidermal water loss⁴¹. Linoleic acid is the most used in dermo-cosmetic formulations, reducing transepidermal water loss and increasing skin moisture because it improves the healing process of sunburn and dermatoses⁴².

CONCLUSION:

Studies on vegetable oils that are rich in essential fatty acids have shown that the components of these oils, particularly the fatty acids, can help to increase collagen production and reduce inflammation. While the body can synthesize many fatty acids, some, such as linoleic acid, cannot be synthesized and must be obtained from outside sources. A deficiency in linoleic acid can lead to dry and flaky skin and transepidermal water loss. This research has established that Chenopodium pallidicaule seed oil is an important linoleic acid source, making it a justifiable ingredient in the formulation of dermo-cosmetic preparations. Additionally, this oil has been shown to have antioxidant activity and to inhibit both collagenase and elastase, like other oils that have been previously studied. However, it is essential to conduct further clinical and safety studies to confirm and consolidate the dermatological properties of this oil in patients.

CONFLICT OF INTEREST:

The authors have no conflicts of interest regarding this investigation.

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Received on 26.03.2024 Revised on 15.07.2024

Accepted on 11.10.2024 Published on 24.12.2024

Available online from December 27, 2024

Research J. Pharmacy and Technology. 2024;17(12):5869-5876.

DOI: 10.52711/0974-360X.2024.00891